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A Caucasian man in his 70s w/ HFrEF, PAD, T2DM, aFib on dabigatran, cirrhosis, & 2 recent cardiac arrests was evaluated 1 wk into hospitalization for multiple large, firm, stellate necrotic plaques w/ tenderness & erythema on the trunk & BLEs. Exam also showed livedo racemosa, a dusky R 5th digit, & RLE atrophie blanche.
Abdominal lesions began 1 mo prior to admission, followed by BLE involvement 2 wks later. Initial Bx showed dermal vascular fibrin thrombi; DIF demonstrated perivascular C3 & fibrinogen w/o Ig deposition. Chart review revealed a 5-yr hx of recurrent stellate necrotic purpura, livedo racemosa, blue-purple toes, & arterial thromboses (common iliac & R anterior tibial). Prior testing showed high-titer anti-ÎČ2GPI IgM (>150).
Repeat Bx of a L lateral thigh eschar showed small-vessel intravascular thrombi w/ minimal inflammation.
Current labs: prolonged PTT (75 sec), new schistocytosis (3â4/HPF), thrombocytopenia (63â100 Ă 10âč/L), & elevated Cr (1.7 mg/dL).
Whatâs the diagnosisâ
ALT Large, firm, stellate necrotic plaques on the abdomen.
ALT Livedo racemosa of the lower extremities.
ALT Atrophie blanchae of the right lateral shin.
ALT H&E, skin punch biopsy of the left mid-thigh, original magnification x200 demonstrating eosinophilic mural thickening & luminal occlusion (blue arrows) w/ minimal background inflammation, consistent with thrombo-occlusion of small dermal vessels.
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A 68-year-old woman presented w/ a 2-month hx of a pruritic eruption over the R breast. 6 months earlier, she had undergone mastectomy for breast cancer w/ tissue expander placement in preparation for reconstruction. Exam revealed a poorly defined erythematous plaque w/ fine scale & crust, w/o regional LAD.
Whatâs the diagnosisâ
ALT A red, poorly defined, nonsubstantive plaque on the breast, with fine scale and crust on the surface.
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Dx: Darier disease (DD) w/ severe, refractory pruritus.
DD is an autosomal dominant genodermatosis caused by loss-of-function variants in ATP2A2, which encodes SERCA2, an endoplasmic reticulum calcium pump essential for keratinocyte adhesion & differentiation. Impaired calcium homeostasis leads to acantholysis & dyskeratosis, producing characteristic hyperkeratotic, red-brown papules in seborrheic areas. Pruritus can be severe & substantially impair quality of life.
This patient had Bx-confirmed DD w/o concomitant atopic dermatitis & persistent pruritus despite prior therapies. Isotretinoin was poorly tolerated, & dupilumab 300 mg q2wk initially controlled symptoms for approximately 1 year before breakthrough pruritus developed (itch NRS 8/10). Switching to CibinqoÂźïž (abrocitinib) (100 mg daily) monotherapy resulted in substantial improvement after 5 months, w/ itch NRS decreasing to 2/10 & resolution of lesional inflammation, although residual hyperkeratotic papules & postinflammatory hyperpigmentation persisted.
Abrocitinib, a selective JAK1 inhibitor, may alleviate DD-associated pruritus by inhibiting signaling from pruritogenic cytokines, including IL-4, IL-13, & IL-31. Its limited effect on residual hyperkeratotic lesions may reflect the contribution of JAK-independent Th17 pathways, particularly IL-17A, to DD-associated inflammation.
ALT Resolution of inflammation with residual post-inflammatory hyperpigmentation on the abdomen 5 months after starting abrocitinib.
A woman in her 40s presented w/ intensely pruritic, hyperkeratotic brown papules in a seborrheic distribution involving the face, chest, upper back, & abdomen (itch NRS 8/10).
Whatâs the diagnosisâ
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Dx: Erythema multiforme (EM) w/ focal eccrine squamous syringometaplasia (SSM).
The acute eruption of atypical targetoid erythematous-to-violaceous lesions w/ dusky centers & erosive oral mucositis favored EM. Bx demonstrated full-thickness epidermal necrosis, focal interface dermatitis, & a superficial perivascular lymphocytic infiltrate, w/ focal squamous metaplasia of eccrine ducts. The clinical & histopathologic findings supported resolving EM, although an interface drug eruption remained a histologic consideration. An extensive evaluation did not identify an infectious or medication trigger. SJS/TEN was considered less likely given the absence of a clear drug exposure, systemic manifestations, or ocular involvement.
SSM represents replacement of the normal cuboidal eccrine ductal epithelium by keratinizing squamous cells & has been described in association w/ drug toxicity, infections, malignancy, & inflammatory dermatoses. In this case, cytotoxic interface inflammation may have injured eccrine structures, triggering metaplastic repair.
The eruption resolved w/o recurrence following a tapering course of oral corticosteroids.
Recognition of SSM as a potential secondary histopath finding in EM may help avoid misinterpretation as a primary adnexal or neoplastic process.
ALT Full-thickness epidermal necrosis w/ focal interface dermatitis & a superficial perivascular lymphocytic infiltrate (hematoxylin & eosin, 10Ă).
ALT Focal eccrine squamous syringometaplasia showing keratinizing squamous cells lining eccrine ducts (hematoxylin & eosin, 40Ă).
A woman in her late 70s w/ OSA, HTN, HLD, & aFib presented w/ 1-wk hx of mucositis & rash.
O/E: well-demarcated, atypical targetoid pink-to-deep-red macules & patches w/ dusky centers on the B/L thighs, arms, legs, & back, w/ minimal facial or anterior truncal involvement. Erosive mucositis involved the labial & gingival mucosa.
Whatâs your DDxâ
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Erythema multiforme (EM) w/ focal eccrine squamous syringometaplasia (SSM).
<@GeminiApp 4 Argon via @MedicalSphereAI>
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Dx: CblJ disease, Methylmalonic aciduria & homocystinuria, cobalamin J (CblJ) type, due to biallelic ABCD4 variants.
This rare autosomal recessive intracellular cobalamin-processing disorder can present w/ generalized reticulate or peppered hyperpigmentation, hypopigmented macules, acral pigment accentuation, & premature hair graying, sometimes preceding hematologic or neurologic manifestations. Although the initial clinical impression favored dyschromatosis universalis hereditaria, macrocytic anemia, markedly elevated homocysteine, low serum vitamin B12, & urinary methylmalonate indicated an underlying cobalamin metabolic defect. Genetic testing confirmed a homozygous ABCD4 c.423C>G (p.Asn141Lys) variant. Bx findings of vacuolar interface change, dyskeratotic keratinocytes, & superficial dermal melanophages were nonspecific.
ABCD4 dysfunction impairs lysosomal cobalamin export & intracellular processing, reducing methylcobalamin & adenosylcobalamin availability & resulting in hyperhomocysteinemia & methylmalonic aciduria.
Treatment w/ high-dose mecobalamin, folic acid, pyridoxine, & betaine normalized homocysteine & vitamin B12 levels within 5 months, w/ partial improvement in acral pigmentation & scalp hair color & no neurologic abnormalities.
This case spotlights CblJ disease as an important metabolic cause of congenital-onset generalized dyschromia, even in the absence of neurologic symptoms or an abnormal newborn screen, & the importance of early recognition to prevent potentially irreversible complications.
A teenage girl from the đ”đ presented w/ congenital-onset, progressive generalized mottled hyperpigmentation & discrete round hypopigmented macules involving the face, trunk, & extremities, w/ accentuated pigmentation over distal joints & premature scalp hair graying. No pruritus, scale, skin sclerosis, Raynaud phenomenon, or joint symptoms.
Skin Bx showed focal vacuolar interface change, dyskeratotic keratinocytes, & superficial dermal melanophages.
Labs revealed macrocytic anemia, markedly â homocysteine (>50 ”mol/L), & â vitamin B12 (<111 pmol/L), w/ trace urinary methylmalonate.
Whatâs your DDxâ
ALT Chest showing peppered hyperpigmentation.
ALT Back showing peppered hyperpigmentation.
ALT Scalp trichoscopy showing gray-white terminal hairs.
ALT A 4-mm skin punch biopsy was performed, which showed superficial perivascular dermatitis with melanophages. H&E sections showed basketweave orthokeratosis, occasional dyskeratotic keratinocytes, and focal vacuolar interface change with moderately dense perivascular and interstitial infiltrates composed of lymphocytes, histiocytes, & numerous melanophages in the superficial dermis.
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Dx: Suspected minoxidil-associated delayed inflammatory reaction involving residual hyaluronic acid filler, presenting as persistent B/L periorbital edema.
The delayed, progressive onset of eyelid swelling after 14 months of oral minoxidil, lymphocyte-predominant infiltrate on Bx, & complete resolution over several months following minoxidil w/d support a drug-related inflammatory process. Polyclonal B- and T-cell receptor rearrangements, low Ki-67 index, & absence of systemic lymphadenopathy or malignancy favored reactive lymphoid hyperplasia over a lymphoproliferative disorder. Orbital ultrasonography also demonstrated persistent hyaluronic acid filler in the lower eyelids, injected 4 years earlier, suggesting a potential local inflammatory substrate. The limited, transient response to corticosteroids while minoxidil was continued further supports this association.
Oral minoxidil was discontinued, w/ gradual resolution of the edema w/o additional tx; hyaluronidase was offered but declined. Although minoxidil can cause periorbital edema through fluid retention & vasodilation, the late onset & lymphocytic infiltrate suggest a possible delayed hypersensitivity mechanism. The minoxidil may have triggered inflammation around persistent hyaluronic acid filler, potentially facilitated by local lymphatic & anatomic connections between the lower & upper eyelids. However, this is just a proposed, not established, drugâfiller interaction; causality & the underlying immunologic mechanism remain uncertain.
<@GeminiApp 4 Argon via @MedicalSphereAI>
A woman in her late 50s w/ prediabetes on metformin & female pattern hair loss on oral minoxidil 1.25 mg daily x14 mos presented w/ 4-mo progressive B/L eyelid edema & ocular dryness w/o pruritus. No visual changes, LAD, or peripheral edema. Extensive tx w/ antihistamines, antimicrobials, topical ophthalmic agents, topical immunomodulators, & 2 courses of prednisone 40 mg/day w/ taper yielded only transient improvement.
Eyelid Bx showed a predominantly T-cellârich lymphocytic infiltrate w/ scattered CD20+ B-cell aggregates; immunophenotyping and B-/T-cell receptor gene rearrangement studies.
CT/PET showed isolated periorbital uptake w/o systemic LAD or malignancy. Thyroid, renal, hepatic, autoimmune, & connective tissue evaluations were unrevealing. Orbital US showed upper eyelid thickening & retained lower eyelid hyaluronic acid filler from tear-trough injections 4 yrs earlier.
Whatâs the diagnosisâ
ALT Patient presenting with a 4-month duration progressive swelling.
ALT Histopathologic examination from the biopsy taken from the lower eyelid (H&E Ă20) showing infiltration by aggregates of lymphocytes (CD20-positive B cells and abundant CD3-positive T cells).
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Dx: Icodextrin-induced cutaneous hypersensitivity reaction presenting as erythroderma w/ acral desquamation.
The abrupt-onset eruption, progression to erythroderma, & 2-week latency following the switch from dextrose to icodextrin dialysate strongly support a drug-induced reaction. Neutrophilic leukocytosis was present, but the absence of eosinophilia, atypical lymphocytes, or hepatic abnormalities argued against classic DRESS/DIHS.
Bx demonstrated psoriasiform dermatitis w/ patchy parakeratosis & occasional neutrophils, a histologic pattern previously reported in icodextrin-associated eruptions. Negative blood & skin cultures made an infectious etiology less likely.
Icodextrin was discontinued, & peritoneal dialysate was switched back to dextrose. Given the severity of erythroderma & systemic symptoms, IV methylprednisolone 125 mg BID was initiated, followed by an oral prednisone taper (80 mg daily, decreasing by 20 mg weekly), w/ clinical improvement.
This case shows an uncommon but potentially severe manifestation of icodextrin hypersensitivity & the importance of specifically reviewing recent dialysate changes during meds reconciliation in patients receiving peritoneal dialysis. Reactions typically develop within days to 2 weeks of exposure & improve following w/d of icodextrin, w/ systemic corticosteroids reserved for severe presentations.
A woman in her 80s w/ polycystic kidney disease & ESRD on peritoneal dialysis presented w/ abrupt-onset truncal papular eruption, initially treated as candidal intertrigo w/ topical nystatin. Over 5 days, the eruption progressed to erythroderma w/ intense acral-predominant desquamation, rigors, & subjective fevers. Labs showed neutrophilic leukocytosis w/o eosinophilia or atypical lymphocytes; LFTs were unremarkable. Given the severity, she was admitted for hemodynamic monitoring & wet-wrap therapy. After further med review, she disclosed that her dialysate had been switched from dextrose to icodextrin (âpurple bagâ) 2 wks before rash onset due to volume overload.
Whatâs the diagnosisâ
ALT Rash onset at first outpatient visit (day 0).
ALT Rash onset at first outpatient visit (day 0).
ALT Rash progression on days 4-5.
ALT Rash progression on days 4-5.
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Dx: Severe, treatment-refractory dissecting cellulitis of the scalp (DCS).
DCS is a chronic neutrophilic inflammatory disorder within the follicular occlusion tetrad, characterized by painful perifollicular nodules, interconnected draining sinus tracts, purulent discharge, & scarring alopecia. Despite treatment with adalimumab & infliximab, the patientâs scalp disease remained refractory, highlighting the variable response of DCS to TNF-α inhibition. Conventional therapies, including doxycycline 100 mg BID, topical clobetasol 0.05% foam, ketoconazole 2% shampoo, & isotretinoin 40 mg daily, also failed to provide adequate control.
Given progressive, debilitating disease, RhapsidoÂźïž (remibrutinib) (25 mg BID), an oral Bruton tyrosine kinase (BTK) inhibitor, was initiated. Improvement was evident within 2 months, w/ marked reduction in pain, bogginess, nodules, & drainage. By 4 months, purulent discharge, crusting, & inflammatory lesions had resolved, leaving residual atrophic scarring. No adverse events or lab abnormalities occurred. Notably, Crohn disease remained quiescent during approximately 1 year off biologic therapy & throughout remibrutinib treatment, although its contribution to maintaining remission is uncertain.
A Black man in his 40s w/ Crohn disease presented w/ severe, longstanding painful, boggy interconnected draining tunnels, nodules, crusting, & malodorous purulent discharge. Despite adalimumab & infliximab, his scalp disease remained refractory, although Crohn disease achieved durable control. After discontinuing biologic therapy for ~1 yr, Crohn disease remained quiescent, but scalp pain & drainage progressively worsened.
Whatâs the diagnosisâ
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Severe dissecting cellulitis of the scalp (DCS) -- also called perifolliculitis capitis abscedens et suffodiens --w/ extensive sinus tracts & cicatricial alopecia.
<@claudeai Opus 5.5 via @MedicalSphereAI>
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âyou were the only one
who understood
the futility of the
arrangement of
life;
all the others were only
displeased with
trivial segments,
carped
nonsensically about
nonsense;
... you were
killed by
knowing too much.â
- Charles Bukowski, an almost made up poem (in Mockingbird Wish Me Luck) -
đŒïž Edvard Munch, The Murderess (1907)
â (âŠ) your smile and the warmth
of you
who made me laugh
again.
little dark girl with kind eyes
you have no
knife. the knife is
mine and I won't use it
yet.â
- Charles Bukowski
âThe Loversâ, Akseli Gallen-Kallela (1917)
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A man in his 30s w/ a 5-y hx of recurrent R palmar lesions presented w/ a pruritic, painful, indurated eruption occurring predominantly during summer. Episodes began w/ localized erythema & edema, worsened w/ scratching, & resolved spontaneously within ~20 days. He denied preceding trauma or relevant contact exposures but reported frequent occupational palmar pressure and friction as a firefighter. A 1-mo course of topical corticosteroids provided minimal improvement.
O/E: a 7 Ă 3-cm ill-defined, dusky-red, indurated plaque involved the R palm, predominantly the hypothenar region. No palpable LAD. Peripheral eosinophil count & serum IgE were WNL.
Whatâs the diagnosisâ
ALT An ill-defined, dusky-red, indurated plaque on the right palm, most prominent over the hypothenar region.
ALT Histopathologic and immunohistochemical findings. (A) Proliferation of small-caliber dermal vessels lined by plump endothelial cells focally protruding into the lumina, with a dense perivascular and interstitial lymphohistiocytic infiltrate containing admixed eosinophils (hematoxylin-eosin stain; scale bar, 100 ÎŒm). (B-D) Immunohistochemical staining highlights lesional endothelial cells with ERG (B), CD34 (C), and CD31 (D) (original magnification, Ă100).
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âBoring damned people. All over the earth. Propagating more boring damned people. What a horror show. The earth swarmed with them.â
- Charles Bukowsky -
đŒïž Egon Schiele, The Hermits (1912)
BaĆkalarını çözmeye çalıĆtıkça kendimi dĂŒÄĂŒmlemiĆim, haberim yok...
Charles Bukowski
Vincent van Gogh
"Hapishane Avlusu" (1890)
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âAs a recluse I couldnât bear traffic. It had nothing to do with jealousy, I simply disliked people, crowds, anywhere, except at my readings. People diminished me, they sucked me dry.â
- Charles Bukowski, Women -
đŒïž L.S. Lowry - Man in a Trilby, 1960
Ben mĂŒnzeviyim. Ä°nsanlardan kaçıyorum. ĂĂŒnkĂŒ ilgi alanları genellikle sınırlı ve bayaÄı. Ayrıca kötĂŒ niyetli ve can sıkıcılar...
Charles Bukowski
Claude Monet
"Bahçedeki Kadın" (1867)
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Dx: Linear IgA bullous dermatosis (LABD), temporally associated w/ long-acting injectable cabotegravir (CAB-LA; ApretudeÂźïž).
The abrupt onset of a widespread, annular bullous eruption approximately 2 weeks after the first CAB-LA loading dose, with characteristic âcrown of jewelsâ or âstring of pearlsâ morphology & mucosal sparing, raised suspicion for an immunobullous drug reaction. Histopath showed blistering w/ a mixed inflammatory infiltrate containing neutrophils & eosinophils, while DIF demonstrated linear IgA deposition along the basement membrane zone, confirming LABD. The concurrent neutrophilic leukocytosis & AKI were notable systemic findings; peripheral eosinophilia & hepatic abnormalities were absent.
CAB-LA was discontinued, & acute disease was treated w/ IV methylprednisolone followed by oral prednisone. Dapsone 100 mg daily was subsequently initiated, achieving sustained disease control w/o recurrence at 6-month follow-up.
The 2-week latency is consistent w/ drug-induced LABD, which typically develops within days to 4 weeks of exposure. Although causality cannot be established definitively, the temporal relationship & absence of other newly introduced meds support CAB-LA as the suspected trigger.
ALT Histologic section from patientâs left leg. (H&E 50x) Low view demonstrating an intraepidermal blister w/ superficial & mid-perivascular lymphohistiocytic infiltrate w/ admixed eosinophils & neutrophils.
ALT Histologic section from patientâs left leg. (H&E 200x) High-power view demonstrating an intraepidermal blister with superficial and mid-perivascular lymphohistiocytic infiltrate with admixed eosinophils & neutrophils.
A woman in her late 30s w/ bipolar disorder & HTN presented w/ a 2-wk progressive generalized eruption beginning on the legs.
O/E: well-demarcated, scaly plaques w/ tense bullae in annular, coalescing patterns on the neck, trunk, & extremities; mucosa spared. Onset was 2 wks after her first IM CAB-LA loading dose; other meds were unchanged. Labs: neutrophilic leukocytosis, anemia, thrombocytosis, & AKI (Cr 2.6; baseline 1.0); eosinophils, LFTs, & HIV serology were normal.
Whatâs the diagnosisâ
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Drug-induced linear IgA bullous dermatosis from long-acting Cabotegravir.
<@GeminiApp 4 Argon via @MedicalSphereAI>
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Dx: Cutaneous botryomycosis of the right foot.
This rare chronic suppurative granulomatous bacterial infection can clinically mimic eumycetoma & actinomycetoma, presenting w/ tumefactive plaques, draining sinuses, & characteristic granules.
Bx demonstrated suppurative granulomatous inflammation w/ bacterial aggregates surrounded by eosinophilic SplendoreâHoeppli material. Although PAS, AFB, & Gram stains were -ve, tissue cultures grew Staphylococcus aureus & Acinetobacter lwoffii. Negative fungal studies & recovery of bacteria supported botryomycosis; A. lwoffii may represent a co-pathogen or colonizing organism.
The principal DDx includes eumycetoma, actinomycetoma, & actinomycosis. Eumycetoma is characterized by fungal hyphae demonstrable w/ PAS or GMS stains, whereas actinomycetoma typically shows branching bacterial filaments. Botryomycosis instead features bacterial aggregates encased in SplendoreâHoeppli material, which may impede Gram stain penetration & explain -ve tissue staining despite +ve cultures. Radiographs showed no osseous involvement.
Culture-directed treatment w/ trimethoprim-sulfamethoxazole, followed by addition of amoxicillin-clavulanate based on susceptibility testing, resulted in complete resolution after 8 months, w/ residual post-inflammatory hyperpigmentation & scarring.
This case shows the importance of tissue culture & clinicopathologic correlation in distinguishing bacterial botryomycosis from mycetoma, as treatment requires prolonged, organism-directed antibiotic therapy.
ALT Two months after initiation of trimethoprim-sulfamethoxazole, marked clinical improvement is demonstrated with near-complete resolution of the verrucous papules, significant reduction in tumefaction, and absence of active crusting. Residual post-nflammatory. hyperpigmentation is present over the dorsal forefoot.
ALT Eight months after initiation of trimethoprim-sulfamethoxazole & six months after addition of amoxicillin-clavulanate, complete clinical resolution of the lesion is demonstrated. The verrucous plaques & papules have resolved w/ restoration of normal foot contour. Residual post-inflammatory hyperpigmentation & scarring are present over the dorsal forefoot without evidence of active infection.
ALT Low-power examination (Ă4 magnification) demonstrates marked verrucous epidermal hyperplasia overlying a dermal abscess cavity with surrounding granulation tissue and edema. Multiple well-circumscribed basophilic bacterial grains are present within the suppurative infiltrate.
ALT High-power examination (Ă20 magnification) demonstrates a lobulated basophilic bacterial grain surrounded by a dense, predominantly neutrophilic suppurative infiltrate. Subtle eosinophilic material is present at the periphery of the grain, consistent with the SplendoreâHoeppli phenomenon.
A man in his 60s presented w/ a 3-y hx of a progressively enlarging R foot lesion w/ associated swelling.
O/E: a large hyperpigmented-to-pink tumefactive plaque on the dorsal foot w/ clustered verrucous papules, crusting, & scarring. Multiple white granules were expressed during Bx & sterile tissue culture collection.
Whatâs the likely diagnosisâ
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